Attenuation by acetaminophen or arachidonic acid-induced coronary vasodilation and output of prostaglandins in the isolated rat heart.
We studied the effect of acetaminophen on the vascular actions of arachidonic acid and on the output of prostaglandins in the isolated rat heart. Arachidonic acid (33 nmol), administered as a bolus into the heart through the aortic cannula produced vasoconstriction followed by a long lasting vasodilation. Arachidonic acid also markedly increased the output of PGE2 and 6-keto-PGF1 alpha from the heart. In the presence of acetaminophen (0.1-1.0 mM) both the output of prostaglandins and the duration of the coronary vasodilation were attenuated. We suggest that the major component of arachidonic acid-induced coronary vasodilation is mediated through prostaglandin synthesis and is blocked by acetaminophen.
D015121:6-Ketoprostaglandin F1 alpha; D000082:Acetaminophen / Q000494:pharmacology*; D000818:Animals; D016718:Arachidonic Acid; D001095:Arachidonic Acids / Q000494:pharmacology*; D006321:Heart / Q000187:drug effects* / Q000502:physiology; D066298:In Vitro Techniques; D008297:Male; D010477:Perfusion; D011453:Prostaglandins / Q000096:biosynthesis*; D011458:Prostaglandins E / Q000096:biosynthesis; D011460:Prostaglandins F / Q000096:biosynthesis / Q000378:metabolism; D051381:Rats; D014664:Vasodilation / Q000187:drug effects*
D001095:Arachidonic Acids; D011453:Prostaglandins; D011458:Prostaglandins E; D011460:Prostaglandins F; D016718:Arachidonic Acid; D000082:Acetaminophen; D015121:6-Ketoprostaglandin F1 alpha